Biochemical events/changes

Glucocorticoids not only break down protein but also stimulate the catabolism of lipids in adipose tissue and enhance the actions of other lipolytic agents. This occurrence results in an increase in plasma free fatty acids and an enhanced tendency to ketosis. The mechanism of this lipolytic action is unknown. The net effect of the biochemical changes induced by the glucocorticoids is antagonism of the actions of insulin. These biochemical events promote hyperglycemia and glycosuria, which are similar to the diabetic state. 

During ripening, three primary biochemical events occur, glycolysis, lipolysis and proteolysis. The products of these primary reactions undergo numerous modifications and interactions. The primary reactions are fairly well characterized but the secondary changes in most varieties are more or less unknown. An overview of the principal biochemical changes follows. 

Binding leads to one of two consequences. If the receptor is coupled to an ion channel, the channel is opened, ions move down electrochemical gradients, and the membrane potential is changed. If the receptor is linked to a G protein, the binding initiates a sequence of biochemical events that result in the production of a second messenger such as cAMP or IP3. These evoke long-term changes that alter excitability of the postsynaptic cell. The complexation process is usually rapidly reversible with an occupancy half-life of 1-20 ms. 

Before a cell can divide, it must essentially double its mass and duplicate all of its contents, so that the two new daughter cells have all the components to initiate their own cycles of cell growth and division. Because the events of nuclear division (mitosis) and cytoplasmic division (cytokinesis) produced dramatic morphologic changes readily seen with the light microscope, earlier studies focused on these relatively brief events. In the time between divisions (interphase), little seemed to be happening. We now know that most of the biochemical events in preparation for division occur continuously throughout interphase. 

Enzyme Changes without Identification of a Prime Biochemical Event... 

The mechanisms of the changes in cell viability during renal injury are incompletely understood. Most of the experimental data have been derived from the ischemia-reperfusion model of acute kidney injury and have focused on necrotic cell death. Because as many as 50% of patients have ischemia-induced acute kidney injury, the observations should be relevant to a large portion of the patients at risk. Also, different stresses initiate common biochemical events, so that understanding the relevant pathways of one stress will most likely be apphcable to others. What follows is a detailed analysis of some of the pathways currently thought to execute cell death in a variety of nephrotoxic insults. 

Adrenoceptors are proteins embedded in the cell membrane that are coupled through a G-protein to effector mechanisms that translate conformational changes caused by activation of the receptor into a biochemical event within the cell. All of the )3-adrenoceptors are coupled through specific G-proteins (Gg) to the activation of adenylyl cyclase (45). When the receptor is stimulated by an agonist, adenylyl cyclase is activated to catalyze conversion of ATP to cyclic-adenosine monophosphate (cAMP), which diffuses through the cell for at least short distances to modulate biochemical events remote from the synaptic cleft. Modu-lationof biochemical events by cAMP includes a phosphorylation cascade of other proteins. cAMP is rapidly deactivated by hydrolysis of the phosphodiester bond by the enzyme phosphodiesterase. The a,-receptor may use more than one effector system, depending on the location of the receptor however, to date the best understood effector system of the a,-receptor appears to be similar to that of the )3-re-... 

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